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Invasive ship rats (Rattus rattus) are a major threat to the native species and ecosystems of islands. We used 10 self-resetting traps (A24 rat and stoat traps, Goodnature Ltd., Wellington, NZ), along with existing single kill DOC200 traps at two devices per hectare on a 9.3 hectare island in New Zealand to reduce rat numbers and ideally achieve eradication. Each self-resetting trap was monitored with motion-activated cameras to analyse rat behaviour and A24 kill numbers were documented using Goodnature digital strike counters. The traps were checked on 10 occasions from August 2016 to October 2017. The videos documented initial high rat activity on the island, which reduced over time following initial trapping success. An immediately obvious neophobic response towards the A24 traps was not observed. Rats interacted with the A24 traps within hours after initial deployment and 60% of the traps were triggered in the first night. After three nights, all traps were triggered at least once. While rats interacted with the traps at all times of the year the number of observed trap-triggers was relatively low. High number of interactions resulted in high kill numbers in late spring when population size was increasing and seasonal food abundance had not yet reached its peak. A second peak was observed in late autumn when rat abundance was presumably high. Recruitment of naïve individuals was a probable cause for high kill numbers during the breeding season. In winter, when rat abundance was presumably low, a few individuals were the likely cause for a high number of interactions while kill numbers were low. A knock-down (i.e. suppression from high to low abundance) of rats using both trap types was achieved in the first 100 days. However, kill numbers of A24s declined over time. After the initial suppression, the number of rats killed was insufficient to offset intrinsic population growth and reinvasion from the adjacent coast, thereby preventing eradication. [ABSTRACT FROM AUTHOR]

Rimonabant (SR 141716) is a specific antagonist of the cannabinoid- 1 receptor. Activation of the receptor initiates multiple effects on central nervous system function, metabolism, and body weight. The hypothesis that rimonabant has protective effects against vascular disease associated with the metabolic syndrome was tested using JCR:LA-cp rats. JCR:LA-cp rats are obese if they are cp/cp, insulin resistant, and exhibit associated micro- and macrovascular disease with end-stage myocardial and renal disease. Treatment of obese rats with rimonabant (10 mg x [kg.sup.-1] x [day.sup.-1], 12-24 wk of age) caused transient reduction in food intake for 2 wk, without reduction in body weight. However, by 4 wk, there was a modest, sustained reduction in weight gain. Glycemic control improved marginally compared with controls, but at the expense of increased insulin concentration. In contrast, rimonabant normalized fasting plasma triglyceride and reduced plasma plasminogen activator inhibitor-1 and acute phase protein haptoglobin in cp/cp rats. Furthermore, these changes were accompanied by reduced postprandial intestinal lymphatic secretion of apolipoprotein B48, cholesterol, and haptoglobin. While macrovascular dysfunction and ischemic myocardial lesion frequency were unaffected by rimonabant treatment, both microalbuminuria and glomerular sclerosis were substantially reduced. In summary, rimonabant has a modest effect on body weight in freely eating obese rats and markedly reduces plasma triglyceride levels and microvascular disease, in part due to changes in intestinal metabolism, including lymphatic secretion of apolipoprotein B48 and haptoglobin. We conclude that rimonabant improves renal disease and intestinal lipid oversecretion associated with an animal model of the metabolic syndrome that appears to be independent of hyperinsulinemia or macrovascular dysfunction. metabolic syndrome; chylomicron overproduction; inflammation; microalbuminuria; glomerular sclerosis; plasminogen activator inhibitor-1; apolipoprotein B48 doi: 10.1152/ajpgi.00173.2010.

House mice (Mus musculus) are an invasive species on Auckland Island in the New Zealand subantarctic and planning for their eradication is underway. Mast seeding events cause rodent populations to irrupt, though little is known about this phenomenon in snow tussock grass (Chionochloa spp.) systems on Southern Ocean islands. The aim of this study was to understand population fluctuations of mouse abundance on Auckland Island for the 2 years following a mast event, and with which tools to monitor abundance, to inform planning of bait application for eradication. Mouse populations were studied using kill and live trapping at two sites on Auckland Island, and mouse density was estimated using spatially explicit capture-recapture models. Mouse population density was highest during summer mast seeding of Chionochloa antarctica and then declined the following winter and subsequently remained low for the following year. Breeding remained seasonal, with a pulse in early summer and a very low level continuing through winter in both years, regardless of mast conditions. These results are similar to those from other cool temperate Southern Ocean islands where seasonal resource availability appears to drive breeding. Throughout the study the capture probability of mice was generally higher when population density was lower, which highlights that conclusions about population trends could be misleading if abundance indices are not calibrated to measures of population density. Mouse eradication should preferentially take place outside of a mast event but would likely still succeed during and following a mast event. Our work fills a key knowledge gap about rodent population trends during mast events for Southern Ocean islands, which is particularly important where eradications are planned. [ABSTRACT FROM AUTHOR]

Antipodes Island is part of New Zealand’s World Heritage subantarctic region and hosts special biodiversity values and significant species endemism. Invasive house mice were the only introduced mammal and detrimentally impacted invertebrate and native bird communities. Eradication of mice from Antipodes Island was undertaken in 2016 and confirmed in 2018. We present the monitoring used to confirm eradication of mice and the ecological outcomes measured over the 6 years since the eradication. Result monitoring for confirmation applied a simple regime to search for mice following a delay of two mouse breeding seasons since baiting was completed. Outcome monitoring targeted endemic land bird taxa for possible changes due to operational impacts and ecological recovery following eradication of mice. The operation had no longterm negative impacts and endemic land bird taxa have recovered quickly from variable levels of non-target mortality. Estimates of abundance of Antipodes Island snipe, Antipodes Island pipit and Reischek’s parakeet showed strong long-term positive response to mouse eradication. [ABSTRACT FROM AUTHOR]

Rats of the JCR: LA-cp strain, which are homozygous for the cp gene (cp/cp), are obese, insulin-resistant, and hyperinsulinemic. They exhibit associated micro- and macrovascular disease and end-stage ischemic myocardial lesions and are highly stress sensitive. We subjected male cp/cp rats to pair feeding (providing the rats each day with the amount of food eaten by matched freely fed animals), a procedure that alters the diurnal feeding pattern, leading to a state of intermittent caloric restriction. Effects on insulin, glucose, and lipid metabolism, response to restraint stress, aortic contractile/relaxant response, and myocardial lesion frequency were investigated. Pair-fed young (12-wk-old) cp/cp rats had lower insulin and glucose levels (basal and following restraint), consistent with increased insulin sensitivity, but a greater increase in plasma nonesterified fatty acids in response to restraint. These effects were unrelated to lipolytic rates in adipose tissue but may be related to reduced fatty acid oxidation in skeletal muscle. Older (24-wk-old) pair-fed cp/cp rats had significantly reduced plasma triglyceride levels, improved micro- and macrovascular function, and reduced severity of ischemic myocardial lesions. These changes indicate a significant amelioration of end-stage disease processes in this animal model and the complexity of metabolic/physiological responses in studies involving alterations in food intake. The effects illustrate the sensitivity of the JCR:LA-cp rat, an animal model for the metabolic syndrome and associated cardiovascular disease, to the environmental and experimental milieu. Similar stress-related mechanisms may play a role in metabolically induced cardiovascular disease in susceptible human beings. metabolic syndrome; stress; fatty acids; vascular function; myocardial lesions doi: 10.1152/ajpendo.90257.2008.

Chromium is one of the few trace minerals for which a specific cellular mechanism of action has not been identified. Recent in vitro studies suggest that chromium supplementation may improve insulin sensitivity by enhancing insulin receptor signaling, but this has not been demonstrated in vivo. We investigated the effect of chromium supplementation on insulin receptor signaling in an insulin-resistant rat model, the JCR:LA-corpulent rat. Male JCR:LA-cp rats (4 mo of age) were randomly assigned to receive chromium picolinate (CrPic) (obese n = 6, lean n = 5) or vehicle (obese n = 5, lean n = 5) for 3 mo. The CrPic was provided in the water, and based on calculated water intake, rats randomized to CrPic received 80 [micro]g/(kg*d). At the end of the study, skeletal muscle (vastus lateralis) biopsies were obtained at baseline and at 5, 15, and 30 min postinsulin stimulation to assess insulin signaling. Obese rats treated with CrPic had significantly improved glucose disposal rates and demonstrated a significant increase in insulin-stimulated phosphorylation of insulin receptor substrate (IRS)-1 and phosphatidylinositol (PI)-3 kinase activity in skeletal muscle compared with obese controls. The increase in cellular signaling was not associated with increased protein levels of the IRS proteins, PI-3 kinase or Akt. However, protein tyrosine phosphatase 1B (PTP1B) levels were significantly lower in obese rats administered CrPic than obese controls. When corrected for protein content, PTP1B activity was also significantly lower in obese rats administered CrPic than obese controls. Our data suggest that chromium supplementation of obese, insulin-resistant rats may improve insulin action by enhancing intracellular signaling. J. Nutr. 136: 415-420, 2006. KEY WORDS: * cellular signaling * chromium * obesity * insulin resistance

The accumulation of intracellular triacylglycerol (TG) is highly correlated with muscle insulin resistance. However, it is controversial whether the accumulation of TG is the result of increased fatty acid supply, decreased fatty acid oxidation, or both. Because abnormal fatty acid metabolism is a key contributor to the pathogenesis of diabetes-related cardiovascular dysfunction, we examined fatty acid and glucose metabolism in hearts of insulin-resistant JCR:LA-cp rats. Isolated working hearts from insulin-resistant rats had glycolytic rates that were reduced to 50% of lean control levels (P < 0.05). Cardiac TG content was increased by 50% (P < 0.05) in the insulin-resistant rats, but palmitate oxidation rates remained similar between the insulin-resistant and lean control rats. However, plasma fatty acids and TG levels, as well as cardiac fatty acid-binding protein (FABP) expression, were significantly increased in the insulin-resistant rats. AMP-activated protein kinase (AMPK) plays a major role in the regulation of cardiac fatty acid and glucose metabolism. When activated, AMPK increases fatty acid oxidation by inhibiting acetyl-CoA carboxylase (ACC) and reducing malonyl-CoA levels, and it decreases TG content by inhibiting glycerol-3-phosphate acyltransferase (GPAT), the rate-limiting step in TG synthesis. The activation of AMPK also stimulates cardiac glucose uptake and glycolysis. We thus investigated whether a decrease in AMPK activity was responsible for the reduced cardiac glycolysis and increased TG content in the insulin-resistant rats. However, we found no significant difference in AMPK activity. We also found no significant difference in various established downstream targets of AMPK: ACC activity, malonyl-CoA levels, carnitine palmitoyltransferase I activity, or GPAT activity. We conclude that hearts from insulin-resistant JCR:LA-cp rats accumulate substantial TG as a result of increased fatty acid supply rather than from reduced fatty acid oxidation. Furthermore, the accumulation of cardiac TG is associated with a reduction in insulin-stimulated glucose metabolism. AMP-activated protein kinase; glycolysis; acetyl-CoA carboxylase; glycerol-3-phosphate acyltransferase

Human studies suggest that chromium picolinate (CrPic) decreases insulin levels and improves glucose disposal in obese and type 2 diabetic populations. To evaluate whether CrPic may aid in treatment of the insulin resistance syndrome, we assessed its effects in JCR:LA-corpulent rats, a model of this syndrome. Male lean and obese hyperinsulinemic rats were randomly assigned to receive oral CrPic [80 [micro]g/(kg * d); n = 5 or 6, respectively) in water or to control conditions (water, n = 5). After 3 mo, a 120-min intraperitoneal glucose tolerance test (IPGTT) and a 30-min insulin tolerance test were performed. Obese rats administered CrPic had significantly lower fasting insulin levels (1848 [+ or -] 102 vs. 2688 [+ or -] 234 pmol/L; P < 0.001; mean [+ or -] SEM) and significantly improved glucose disappearance (P < 0.001) compared with obese controls. Glucose and insulin areas under the curve for IPGTT were significantly less for obese CrPic-treated rats than in obese controls (P < 0.001). Obese CrPic-treated rats had lower plasma total cholesterol (3.57 [+ or -] 0.28 vs. 4.11 [+ or -] 0.47 mmol/L, P < 0.05) and higher HDL cholesterol levels (1.92 [+ or -] 0.09 vs. 1.37 [+ or -] 0.36 mmol/L, P < 0.01) than obese controls. CrPic did not alter plasma glucose or cholesterol levels in lean rats. Total skeletal muscle glucose transporter (Glut)-4 did not differ among groups; however, CrPic significantly enhanced membrane-associated Glut-4 in obese rats after insulin stimulation. Thus, CrPic supplementation enhances insulin sensitivity and glucose disappearance, and improves lipids in male obese hyperinsulinemic JCR:LA-corpulent rats. KEY WORDS: * insulin * glucose * chromium * lipids * rats

Research was conducted to examine the status of myofibrillar and sarcoplasmic reticulum function in hearts from JCR:LA-cp rats. This type of rat is a model for type II non-insulin-dependent diabetes mellitus, obese, insulin resistant and possesses high levels of circulating glucose. Results argue against the existence of a cardiomyopathy in the diabetic model and indicate that insulin may be an important factor in the cardiomyopathy observed in type I diabetic models.

A study was performed to determine heart responses of JCR/LA-corpulent rats (JCR-LA-cp) to an interval of ischemic insult. JCR/LA-cp rat is a distinguished genetic animal strain with similar characteristics of the type II diabetes in humans. It was believed that JCR-LA-cp hearts have improper regulation of intracellular calcium concentration. Results of the study showed enhanced sensitivity of murine hearts to ischemia-reperfusion injury as the rats grew older. The significance of results was correlated to the type of diabetes to be considered in myocardial dysfunction.